When anticoagulation is indicated following lung transplantation, warfarin has long been the enteral anticoagulant of choice. However, with the advent of direct acting oral anticoagulants (DOACs), there has been a shift in practice toward these newer agents, but there are scant data to aid in anticoagulation decision making as solid organ transplant recipients are poorly represented in the literature. [1][2][3] DOACs have clear advantages over warfarin with more predictable kinetics, fewer drug-drug and drug-food interactions, and do not require therapeutic drug monitoring. 4,5 Furthermore, DOACs do not require peri-procedural bridging which may improve patient safety and reduce length of stay. 6 The lung transplant population has unique characteristics that necessitate caution with integration of DOACs into practice. Drug interactions are common as lung transplant patients are likely to receive concomitant CYP3A4 and P-glycoprotein (P-gp) inhibiting medications. Inhibition of CYP3A4 metabolic activity may decrease metabolism of substrates, such as apixaban, and hence increase serum concentrations. Inhibition of P-gp may increase intestinal absorption as well as systemic distribution of P-gp substrates, including apixaban. In lung transplant, common CYP3A4 inhibitors include azole antifungals and diltiazem. Medications such as cyclosporine, amiodarone, and itraconazole inhibit both CYP3A4 and P-gp. Management of these interactions is complicated by different degrees of CYP3A4 inhibition (eg, voriconazole is a more potent